Effects of Alcohol Withdrawal On Hangover
January 2, 2009 by rainier
The AW syndrome following the cessation of excessive drinking results from compensatory changes in the central nervous system that take place in response to chronically administered depressant substances (in this case, alcohol, or more specifically, ethanol). These changes include lterations in two types of receptors embedded in nerve cell membranes. One receptor type binds with an important chemical messenger (i.e., neurotransmitter) called gamma-aminobutyric acid (GABA), and the other type binds with another neurotransmitter, glutamate.
Both GABA and glutamate are critical in regulating nerve cell activity: GABA is the body’s primary means of inhibiting nerve cell activity, and glutamate is the primary means of exciting it.Following chronic alcohol exposure, the body decreases (i.e., downregulates) the number or sensitivity of GABA receptors and increases (i.e., upregulates) the number or sensitivity of glutamate receptors in an effort to counterbalance
alcohol’s sedative effects. When alcohol is removed from the body, however, the central nervous system and the portion of the nervous system that coordinates response to stress (i.e., the sympathetic nervous system) remain in an unbalanced “overdrive” state (Tsai et al. 1995). Sympathetic nervous system hyperactivity accounts for the tremors, sweating, and tachycardia observed in both hangover and AW syndrome.
Several lines of evidence suggest that a hangover is a mild manifestation of the AW syndrome in non-alcoholdependent drinkers:
First, the signs and symptoms of hangover and mild AW overlap considerably. The revised Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) scale, an instrument widely used to assess the severity of a withdrawal episode in alcohol-dependent patients, measures 10 withdrawal-associated items: nausea and vomiting; tremor; sweating; anxiety; agitation; headache; disturbances in the sense of touch, hearing, and vision (e.g., hallucinations); and orientation (e.g., awareness of the date and location) (Sullivan et al. 1989, see also p. 8 of the article by Saitz for a sample of the assessment form). Several of these items also are usually present during a hangover, including nausea and vomiting, tremor, sweating, anxiety,headache, and sensory disturbances.
Second, Begleiter and colleagues (1974) present evidence that the hangover condition is actually a state of central nervous system excitation, despite the perceived sedation and malaise. Support for this view comes from the research of Pinel and Mucha (1980), which shows that single doses of alcohol decrease seizure thresholds in animals several hours later. Their finding indicates rebound excitation, a phenomenon noted to occur after short-term administration of some sedatives that can quickly clear the body, including alcohol and certain benzodiazepine drugs.
Third, the observation that alcohol readministration alleviates the unpleasantness of both AW syndrome and hangovers suggests that the two experiences share a common process.
